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Pure Appl. Chem., Vol. 70, No. 9, pp. 1685-1701, 1998

    Natural and anthropogenic environmental oestrogens:
    the scientific basis for risk assessment

    Environmental estrogens and male infertility

    R.M. Sharpe
    MRC Reproductive Biology Unit, Centre for Reproductive Biology, 37 Chalmers Street, Edinburgh EH3 9EW Scotland, UK.
    E-mail: [email protected]

    Introduction: The topics of adverse changes in human male reproductive health (fall in sperm counts, increase in the incidence of testicular cancer, cryptorchidism and hypospadias) and that of 'environmental estrogens', have attracted enormous scientific, public and governmental attention over the past 6 or so years. Though the two topics have invariably been linked together in a postulated cause and effect manner, there is only circumstantial evidence to support such a relationship (35, 76). Whilst such 'absence of data' should not be interpreted as proof that such a causal relationship does not exist (see Table 1), it should also make us circumspect in dealing with this issue and cause us to use scientific rather than emotional criteria when judging or 'weighing' the relevant data. From these introductory remarks it should be clear already to the reader that I will be unable to offer any proof that environmental estrogens either do or do not affect human male fertility. Whilst this may be less than ideal, it should not cause us to lose sight of three important facts. First, adverse trends in male reproductive health have occurred over the past 50 years, although the extent of this change and whether it is truly worldwide are more debatable (75). Second, a biologically plausible case can be made for environmental estrogens inducing adverse changes in male reproductive health (Table 1; ref 69), although plausibility does not tell us anything about likelihood (65). Third, there is no doubt that human exposure to environmental estrogens has altered considerably in the past 50 years, although we do not have accurate measures of how great this change has been nor what relative impact it has had on 'total estrogen exposure' of the individual (45, 76). This chapter will attempt to summarise our current understanding on each of these points and in doing so will hopefully highlight the strengths and weaknesses of the arguments which relate these three topics one to another.

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